Deoxyadenosine triphosphate

Health effects

High levels of dATP can be toxic and result in impaired immune function, since dATP acts as a noncompetitive inhibitor for the DNA synthesis enzyme ribonucleotide reductase. Patients with adenosine deaminase deficiency (ADA) tend to have elevated intracellular dATP concentrations because adenosine deaminase normally curbs adenosine levels by converting it into inosine. Deficiency of this deaminase also causes immunodeficiency.

In cardiac myosin, dATP is an alternative to ATP as an energy substrate for facilitating cross-bridge formation.

References

References

1. (July 1982). "A study of the mechanism of T4 DNA polymerase with diastereomeric phosphorothioate analogues of deoxyadenosine triphosphate". The Journal of Biological Chemistry.
2. (1985-04-01). "Enzymic synthesis of deoxyATP using DNA as starting material". The Journal of Organic Chemistry.
3. (October 1980). "Effects of deoxyadenosine triphosphate and 9-beta-D-arabinofuranosyl-adenine 5'-triphosphate on human ribonucleotide reductase from Molt-4F cells and the concept of "self-potentiation"". Cancer Research.
4. (January 1978). "Deoxyadenosine triphosphate as a potentially toxic metabolite in adenosine deaminase deficiency". Proceedings of the National Academy of Sciences of the United States of America.
5. (May 2007). "Carrier frequency of a nonsense mutation in the adenosine deaminase (ADA) gene implies a high incidence of ADA-deficient severe combined immunodeficiency (SCID) in Somalia and a single, common haplotype indicates common ancestry". Annals of Human Genetics.
6. (January 2016). "2-Deoxyadenosine triphosphate restores the contractile function of cardiac myofibril from adult dogs with naturally occurring dilated cardiomyopathy". American Journal of Physiology. Heart and Circulatory Physiology.
7. (June 2019). "Cardiac myosin activation with 2-deoxy-ATP via increased electrostatic interactions with actin". Proceedings of the National Academy of Sciences of the United States of America.